尿酸の傍細胞経路による輸送の分子メカニズム

Since charged molecule cannot permeate cell membrane, urate movement across the epithelial cell layer has to be transcellularly by carrier or endocytosis/exocytosis, or paracellularly. We have reported that the paracellular route is the major urate transport pathway across the blood-placental barrie...

Full description

Saved in:
Bibliographic Details
Published in日本薬理学会年会要旨集 p. 1-P-111
Main Authors 櫻井, 裕之, 塚田, 愛, 大槻, 純男, 市田, 公美, 福冨, 俊之, 木村, 徹
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2019
Online AccessGet full text
ISSN2435-4953
DOI10.1254/jpssuppl.92.0_1-P-111

Cover

More Information
Summary:Since charged molecule cannot permeate cell membrane, urate movement across the epithelial cell layer has to be transcellularly by carrier or endocytosis/exocytosis, or paracellularly. We have reported that the paracellular route is the major urate transport pathway across the blood-placental barrier. In this study, the mechanism of urate paracellular transport was investigated in several epithelial cell lines. Very little urate passed through MDCK and LLC-PK1 cell layers. Interestingly, one Caco-2 cell line was urate non-permeable while another Caco-2 cell line was found to be urate-permeable. Urate paracellular movement across the Caco-2 cell layer was partially inhibited by DIDS, which inhibits chloride transport. Detection and quantification of claudin proteins that are important for paracellular transport of ions were performed by LC/MS. Claudin 1, 3, 4, 6, 7 and 12 were detected in urate-permeable cell lines, BeWo and Caco-2 cells. However, overexpression of these claudins in MDCK cells did not increase urate paracellular transport. In conclusion, overexpression of single claudin was not sufficient to make urate-non-permeable cell become urate permeable.
Bibliography:92_1-P-111
ISSN:2435-4953
DOI:10.1254/jpssuppl.92.0_1-P-111